Neuroprotective properties of the natural vitamin E alpha-tocotrienol
BACKGROUND AND PURPOSE: The current work is
based on our previous finding that in neuronal cells, nmol/L concentrations
of alpha-tocotrienol (TCT), but not alpha-tocopherol (TCP), blocked
glutamate-induced death by suppressing early activation of c-Src kinase
and 12-lipoxygenase. METHODS: The single neuron microinjection technique
was used to compare the neuroprotective effects of TCT with that of
the more widely known TCP. Stroke-dependent brain tissue damage was
studied in 12-Lox-deficient mice and spontaneously hypertensive rats
orally supplemented with TCT. RESULTS: Subattomole quantity of TCT,
but not TCP, protected neurons from glutamate challenge. Pharmacological
as well as genetic approaches revealed that 12-Lox is rapidly tyrosine
phosphorylated in the glutamate-challenged neuron and that this phosphorylation
is catalyzed by c-Src. 12-Lox-deficient mice were more resistant to
stroke-induced brain injury than their wild-type controls. Oral supplementation
of TCT to spontaneously hypertensive rats led to increased TCT levels
in the brain. TCT-supplemented rats showed more protection against
stroke-induced injury compared with matched controls. Such protection
was associated with lower c-Src activation and 12-Lox phosphorylation
at the stroke site. CONCLUSIONS: The natural vitamin E, TCT, acts
on key molecular checkpoints to protect against glutamate- and stroke-induced
neurodegeneration. Khanna S, Roy S, Slivka A, et al. Stroke.
2005 Oct;36(10):2258-64.
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